It is known that scar formation is a fibroproliferative tissue response which, depending on the tissue or organ involved, results in the regeneration of the damaged tissue, or in the formation of a fibrotic scar. In addition, cutaneous/mucosal scar formation is an interactive process involving soluble mediators, extracellular matrix components, resident cells (keratinocytes, endothelial cells, fibroblasts and nerve fibres), infiltrating leukocytes, participating differentially and in strict temporal sequence towards the three phases of the scar formation process: inflammation, granulation (tissue formation or proliferative phase) and tissue remodelling.
Hence, the repair process is a dynamic and continuous phenomenon, given that the three phases are temporally coexistent with one another. For example, the inflammatory phase, fundamental for triggering the repair process, initiates abruptly at the instant of tissue damage, but persists both during cutaneous/mucosal re-epithelialisation, and during tissue remodelling (even though with different cellular components with respect to the acute phase), influencing both the catabolic and anabolic processes of the entire repair phenomenon.
Accordingly, the conceptual distinction of the repair process into three phases is only really useful for describing the events, sequentially linked to one another, in terms of the chemical mediators released locally at the site of the lesion, and the cellular components involved. Furthermore, the above distinction is useful for identifying during which phase and depending on which cellular elements and/or soluble mediators, any potential anomalies intervene. For example, such anomalies may relate to: excessive or defective chemotropism and/or the activation of specific cellular stipes at the site of the injury; excessive or defective release of soluble mediators; excessive or defective deposition and/or degradation of extracellular matrix; persistent fibroblastic hyperplasia; persistent microbial contamination, with chronicisation of the inflammatory phase. All the conditions listed above are clinically recognisable as hyper-reactivity and/or hyporeactivity of the tissue repair process in any of its phases, with consequential retardation of the sequentiality of the events and/or blockage of correct scar progression.
Pharmaceutical compositions which may be used in the treatment of ulcerations are known. However, these are not capable of providing a comprehensive treatment for ulcerations allowing rapid and efficient tissue repair. Without being bound to any particular theory, one possible cause may be that said compositions contain a factor which is active on one phase or on a single event within any given stage of the scar forming process, and hence they are not capable of addressing the above mentioned complex phenomena, in their entirety.